Tag: NEET PG

Different types of fatty acid oxidation

Oxidation of odd-chain fatty acids result in the production of which of the following?

A

Acetyl CoA

B

Succinyl CoA

C

Propionyl CoA

D

Malonyl CoA

Q. 1

Oxidation of odd-chain fatty acids result in the production of which of the following?

A

Acetyl CoA

B

Succinyl CoA

C

Propionyl CoA

D

Malonyl CoA

Ans.

C

Explanation:

Odd chain fatty acids are also oxidised exactly as even chain fatty acids. However, after successive removal of 2-carbon units, at the end, one 3 carbon unit, propionyl CoA is produced. The propionyl CoA is further metabolised to Succinyl CoA which enters the TCA cycle.

Ref: Vasudevan Biochemistry, 3rd Edition, Page 124

Q. 2

Fatty acid with even number of carbon atoms on oxidation produces:

A

Acetyl CoA

B

Succinyl CoA

C

Propionyl CoA

D

All of the above

Q. 2

Fatty acid with even number of carbon atoms on oxidation produces:

A

Acetyl CoA

B

Succinyl CoA

C

Propionyl CoA

D

All of the above

Ans.

A

Explanation:

Fatty acids with an odd number of carbon atoms are oxidized by the pathway of β-oxidation, producing acetyl-CoA, until a three-carbon (propionyl-CoA) residue remains. This compound is converted to succinyl-CoA, a constituent of the citric acid cycle. Hence, the propionyl residue from an odd-chain fatty acid is the only part of a fatty acid that is glucogenic

Ref: Harper 28th edition, chapter 22.

Q. 3

Very long chain fatty acid is oxidised in:

A

Mitochondria

B

Cytoplasm

C

Peroxisome

D

All of the above

Q. 3

Very long chain fatty acid is oxidised in:

A

Mitochondria

B

Cytoplasm

C

Peroxisome

D

All of the above

Ans.

C

Explanation:

A modified form of oxidation is found in peroxisomes and leads to the formation of acetyl-CoA and H2O2 (from the flavoprotein-linked dehydrogenase step), which is broken down by catalase.

Thus, this dehydrogenation in peroxisomes is not linked directly to phosphorylation and the generation of ATP. The system facilitates the oxidation of very long chain fatty acids (eg, C20, C22).

These enzymes are induced by high-fat diets and in some species by hypo-lipidemic drugs such as clofibrate.

Ref: Harper 28th edition, chapter 22.

Q. 4

Beta-oxidation of odd-chain fatty acids produces:

A

Acetyl CoA

B

Malonyl CoA

C

Succinyl CoA

D

Propionyl CoA

Q. 4

Beta-oxidation of odd-chain fatty acids produces:

A

Acetyl CoA

B

Malonyl CoA

C

Succinyl CoA

D

Propionyl CoA

Ans.

D

Explanation:

Odd chain fatty acids are oxidized in the similar manner as of even chain fatty acid, beta-oxidation.

However, unlike even chain fatty acids which yields only acetyl CoA, odd chain fatty acids will yield Acetyl-CoA and one three carbon acid, Propionyl-CoA.

Propionyl CoA is further converted into succinyl CoA. Fatty acids are an important source of energy. ?Oxidation is the process where energy is produced by degradation of fatty acids.

Beta Oxidation of fatty acids: The pathway for catabolism of fatty acids is referred to as the b-oxidation pathway, because oxidation occurs at the b-carbon (C-3).

Step IV – Thiolytic clevage Thiolase:? cleavage of the two carbon fragment by splitting the bond between α and β carbons, by thiolase enzyme.

Beta oxidation of odd chain fatty acids:

Fatty acids that enter beta-oxidation with an even number of carbons are converted entirely to acetyl-CoA. The beta-oxidation of odd chain fatty acid results in a acetyl-CoA and the 3-carbon chain propionyl-CoA. Propionyl Coa is further converted to succinyl CoA.

Ref: Harper’s, Illustrated Biochemistry, 26th edition, Page 182

Q. 5

β-oxidation of odd-chain fatty acids produces:

A

Succinyl CoA

B

Propionyl CoA

C

Acetyl CoA

D

Malonyl CoA

Q. 5

β-oxidation of odd-chain fatty acids produces:

A

Succinyl CoA

B

Propionyl CoA

C

Acetyl CoA

D

Malonyl CoA

Ans.

B

Explanation:

B i.e. Propionyl CoA

13- oxidation of odd chain fatty acid produces acetyl CoA plus a molecule of propionyl –CoAQ. But propionyl CoA is formed only in odd chain fatty acid oxidation (not in even fatty acids)

Q. 6

Short chain fatty acid produced by bacteria are maximally absorbed in :

A

Duodenum

B

Colon

C

Ileum

D

Jejunum

Q. 6

Short chain fatty acid produced by bacteria are maximally absorbed in :

A

Duodenum

B

Colon

C

Ileum

D

Jejunum

Ans.

B

Explanation:

B i.e. Colon

Major fat absorption takes place in upper small intestine except (mainly jejunum & duodenum) short chain fatty acids which is absorbed in colon0.

Normal fecal fat excretion is less than 6gm/day, more than 6gm/day indicates malabsorptionQ.

Rapoport Leubering cycle

The phenomenon of cancer cells switching to glycolysis even in the presence of adequate oxygen for oxidative phosphorylation is known as:

A

Tyndall effect

B

Warburg effect

C

Hawthorne effect

D

None of the above

Q. 1

The phenomenon of cancer cells switching to glycolysis even in the presence of adequate oxygen for oxidative phosphorylation is known as:

A

Tyndall effect

B

Warburg effect

C

Hawthorne effect

D

None of the above

Ans.

B

Explanation:

Even in the presence of ample oxygen, cancer cells shift their glucose metabolism away from the oxygen hungry, but efficient, mitochondria to glycolysis.

This phenomenon, called the Warburg effect and also known as aerobic glycolysis, has been recognized for many years (indeed, Otto Warburg received the Nobel Prize for discovery of the effect that bears his name in 1931), but was largely neglected until recently.

This metabolic alteration is so common to tumors that some would call it the eighth hallmark of cancer.

Ref: Robbins 8th edition Chapter 2.

Q. 2

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

A

Hypoxia stimulates pyruvate dehydrogenase by increased 2,3 DPG

B

Hypoxia inhibits hexokinase

C

Hypoxia stimulates release of all glycolytic enzymes from band 3 on RBC membrane

D

Activation of the regulatory enzymes by high PH

Q. 2

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

A

Hypoxia stimulates pyruvate dehydrogenase by increased 2,3 DPG

B

Hypoxia inhibits hexokinase

C

Hypoxia stimulates release of all glycolytic enzymes from band 3 on RBC membrane

D

Activation of the regulatory enzymes by high PH

Ans.

C

Explanation:

During Hypoxia, the glycolytic enzymes that bind in the same region of band 3 of Hb are released from the membrane resulting in an increased rate of glycolysis. Increased glycolysis increases ATP production and the hypoxic release of ATP.

Band 3, is a multifunction RBC transmembrane protein, which is important for its cytoskeletal structure, cell shape, anion exchange activity and glycolysisQ. Band 3 is responsible for chloride shift in RBCQ. Hypoxic deoxygenation of hemoglobin causes Band 3 tyrosine phosphorylation and thereby stimulates glycolysis by releasing glycolytic enzymes from band 3 on RBC membraneQ.

In kidney, I cells contain Band 3, an anion exchange protein in their basolateral cell membrane, which may function as a

A human subject takes part in a nutritional research study. After ingesting a very fatty meal, serum samples are taken for research studies at 1 hour and 3 hours. These studies measure the average diameter of the chylomicrons, showing an average chylomicron diameter of 500 nm at 1 hour, which drops to an average diameter of 150 nm at 3 hours. Where is the enzyme responsible for this change located?

A

Adipocytes

B

Endothelial cells

C

Enterocytes

D

Hepatocytes

Q. 4

A human subject takes part in a nutritional research study. After ingesting a very fatty meal, serum samples are taken for research studies at 1 hour and 3 hours. These studies measure the average diameter of the chylomicrons, showing an average chylomicron diameter of 500 nm at 1 hour, which drops to an average diameter of 150 nm at 3 hours. Where is the enzyme responsible for this change located?

A

Adipocytes

B

Endothelial cells

C

Enterocytes

D

Hepatocytes

Ans.

B

Explanation:

Chylomicrons are produced by enterocytes (intestinal epithelial cells), using gut luminal triglycerides for the source of the lipid. The chylomicrons are secreted into the gut lymphatic system, and from there drain eventually into the systemic venous system from the thoracic duct, and hence into the serum portion of the blood. They are initially large and have a very high triglyceride content. With time, lipoprotein lipase releases triglycerides from the chylomicron core by hydrolyzing them to more easily absorbed fatty acids. The enzyme is located on the external surface of the vascular endothelium of tissues with triglyceride needs such as skeletal muscle, cardiac muscle tissue, and lactating breast. The result of lipoprotein lipase activity is that the chylomicrons shrink in size.

While adipose tissue can utilize chylomicrons, lipoprotein lipase is located on the endothelial cells rather than adipocytes. Adipocytes have an adipose tissue lipase, which is an intracellular enzyme that can cleave triglycerides to glycerol and fatty acids, allowing them to be released into the circulation when chylomicrons are low.

Enterocytes have the ability to pick up mixed micelles from the gut lumen for repackaging in the smooth endoplasmic reticulum as chylomicrons.

Hepatocytes pick up the chylomicron remnants after the lipoprotein lipase shrinks them.

The first step in synthesis of steroids is derived from the cleavage of cholesterol. What is the enzyme responsible for the cleavage of 20,22-dehydrocholesterol to pregnenolone?

A

Delta 5-3 beta-hydroxysteroid dehydrogenase (3B – HSD)

B

HMG-CoA reductase

C

Aromatase

D

17 alpha-hydroxylase

Q. 2

The first step in synthesis of steroids is derived from the cleavage of cholesterol. What is the enzyme responsible for the cleavage of 20,22-dehydrocholesterol to pregnenolone?

A

Delta 5-3 beta-hydroxysteroid dehydrogenase (3B – HSD)

B

HMG-CoA reductase

C

Aromatase

D

17 alpha-hydroxylase

Ans.

A

Explanation:

The enzyme responsible for the cleavage of 20,22-dehydrocholesterol to pregnenolone is termed Delta 5-3 beta-hydroxysteroid dehydrogenase ( 3B HSD). Pregnenolone is a precursor to progesterone. Conversion to progesterone is necessary for eventual synthesis of testosterone and estrogen. Although there are different enzymes for their production, progesterone converted from cholesterol is of primary importance.

Which of the following enzymes is common to the synthesis of cholesterol and ketone bodies:

A

HMG -Co-A Reductase

B

HMG-Co-A Lyase

C

HMG-Co-A Synthase

D

Thiokinase

Q. 3

Which of the following enzymes is common to the synthesis of cholesterol and ketone bodies:

A

HMG -Co-A Reductase

B

HMG-Co-A Lyase

C

HMG-Co-A Synthase

D

Thiokinase

Ans.

C

Explanation:

C i.e. HMG-Co-A Synthase

Q. 4

Which of the following blocks DNA replication with getting incorporated in DNA strand:

A

Cytarabine

B

Nalidixic acid

C

Ciprofloxacin

D

Paclitaxel

Q. 4

Which of the following blocks DNA replication with getting incorporated in DNA strand:

A

Cytarabine

B

Nalidixic acid

C

Ciprofloxacin

D

Paclitaxel

Ans.

A

Explanation:

A i.e. Cytarabine

Q. 5

Cholesterol is synthesized from:

A

Acetyl CoA

B

Alpha-ketoglutarate

C

Glutaric acid

D

Oxalate

Q. 5

Cholesterol is synthesized from:

A

Acetyl CoA

B

Alpha-ketoglutarate

C

Glutaric acid

D

Oxalate

Ans.

A

Explanation:

Q. 6

Cholesterol is:

A

Tocopherol

B

Lipoprotein

C

Steroid

D

Lipopolysacchride

Q. 6

Cholesterol is:

A

Tocopherol

B

Lipoprotein

C

Steroid

D

Lipopolysacchride

Ans.

C

Explanation:

Cholesterol is an amphipathic lipid and is an important structural component of membranes and of the outer layer of plasma lipoproteins.

It is mainly synthesized in many tissues from Acetyl-CoA and is the precursor of all other steroids in the body, including corticosteroids, sex hormones, bile acids, and vitamin D.

Q. 7

Cholesterol is not a precursor of:

A

Bile acid

B

Bile pigment

C

Vitamin D

D

Sex hormones

Q. 7

Cholesterol is not a precursor of:

A

Bile acid

B

Bile pigment

C

Vitamin D

D

Sex hormones

Ans.

B

Explanation:

Cholesterol is the precursor of bile acids [Bile contains bile salts (conjugated bile acids), which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, A, D, E, and K].

Q. 8

Mineral required for cholesterol biosynthesis ‑

A

Fe

B

Mn

C

Mg

D

Cu

Q. 8

Mineral required for cholesterol biosynthesis ‑

A

Fe

B

Mn

C

Mg

D

Cu

Ans.

C

Explanation:

Mg is required in stage 2 of cholesterol synthesis.

Biosynthesis (De Novo Synthesis) of cholesterol

The liver is the major site for cholesterol biosynthesis. Some cholesterol is also synthesized in intestine adre‑nal cortex, gonads and skin. The microsomal (smooth endoplasmic reticulum) and cytosol fraction of cell is responsible fir cholesterol synthesis; However most of the reactions in synthesis occurs in cytosol.

Cholesterol is a C-27 compound. All 27-carbon atoms of cholesterol are derived from a single precursor, i.e. acetyl-CoA (activated acetate).

First two molecules of acetyl-CoA condense to form acetoacetyl-CoA. Next, a third molecule of acetyl- CoA condenses with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA). Then HMG-CoA is converted to mevalonate by HMG-CoA reductase, the key regulatory enzyme of cholesterol synthesis.

Metabolism of HDL

Which of the following statements about High Density Lipoprotein (HDL) is false:

A

HDL increases oxidation of LDL

B

HDL reduces foam cell production by LDL

C

HDL is the best predictor of CAD

D

HDL helps to clear lipids from atheromas

Q. 1

Which of the following statements about High Density Lipoprotein (HDL) is false:

A

HDL increases oxidation of LDL

B

HDL reduces foam cell production by LDL

C

HDL is the best predictor of CAD

D

HDL helps to clear lipids from atheromas

Ans.

A

Explanation:

HDL prevent oxidation of LDL in complex in vitro models as a result HDL function as a naturally acting antioxidant which protect vessel wall from oxidative damage and resulting atherogenesis.

Ref: Current Pharmaceutical Design, Page 6.

Q. 2

Good cholesterol found in:

A

HDL

B

LDL

C

VLDL

D

IDL

Q. 2

Good cholesterol found in:

A

HDL

B

LDL

C

VLDL

D

IDL

Ans.

A

Explanation:

A i.e. HDL

HDL contains good cholesterolQ. So there is an inverse relation between HDL (HDL2) concentrations and coronoary heart disease. This is consistent with the function of HDL in reverse cholesterol transport.

Diseases (eg. diabetes mellitus, lipid nephrosis, hypothyroidism and other considtions of hyperlipedimea) in which prolonged elevations of VLDL, IDL, LCD or chulomicron remnants in blood are often accompanied by premature or severe atherosclerosis. This makes LDL : HDL cholesterol ratio a good predective parameter for atherosclerosis & coronary heart disease.

Q. 3

Reverse cholesterol transport is mediated by ‑

A

HDL

B

VLDL

C

LDL

D

IDL

Q. 3

Reverse cholesterol transport is mediated by ‑

A

HDL

B

VLDL

C

LDL

D

IDL

Ans.

A

Explanation:

Ans. is ‘a’ i.e., HDL

Reverse cholesterol transport

All nucleated cells in different tissues synthesize cholesterol, but the excretion of cholesterol is mainly by liver in the bile or by enterocytes in gut lumen.

So, cholesterol must be transported from peripheral tissue to liver for excretion.

o This is facilitated by HDL and is called reverse cholesterol transport because it transports the cholesterol in reverse direction to that is transported from liver to peripheral tissues through VLDL LDL cycle. Process

This nascent HDL is secreted into circulation where it acquires additional unesterified cholesterol from peripheral tissues.

o Within the HDL particle, the cholesterol is esterified by lecithin – cholesterol acetyltransferase (LCAT) to form cholesteryl ester and additional lipid are transported to HDL from VLDL and chylomicrons.

o There are two pathway by which this cholesterol is transported to liver.

Q. 4

All are bad cholesterol except:

A

HDL

B

LDL

C

VLDL

D

IDL

Q. 4

All are bad cholesterol except:

A

HDL

B

LDL

C

VLDL

D

IDL

Ans.

A

Explanation:

HDL can remove cholesterol from atheroma within arteries and transport it back to the liver for excretion or re-utilization, which is the main reason why HDL-bound cholesterol is sometimes called “good cholesterol”, or HDL-C. A high level of HDL-C seems to protect against cardiovascular diseases, and low HDL cholesterol levels (less than 40 mg/ dL or about 1mmol/L) increase the risk for heart disease.

Cholesterol contained in HDL particles is considered beneficial for the cardiovascular health, in contrast to “bad” LDL cholesterol.

Q. 5

Lipoprotein involved in reverse cholesterol transport‑

A

LDL

B

VLDL

C

IDL

D

HDL

Q. 5

Lipoprotein involved in reverse cholesterol transport‑

A

LDL

B

VLDL

C

IDL

D

HDL

Ans.

D

Explanation:

The HDL particles are referred to as scavengers because their primary role is to remove free (unesterified) cholesterol from the extrahepatic tissues.

HDL particles transport cholesterol from extrahepatic tissues to liver (i.e. reverse cholesterol transport) which is then excreted through bile.

Reverse cholesterol transport

All nucleated cells in different tissues synthesize cholesterol, but the excretion of cholesterol is mainly by liver in the bile or by enterocytes in gut lumen. So, cholesterol must be transported from peripheral tissue to liver for excretion. This is facilitated by HDL and is called reverse cholesterol transport because it transports the cholesterol in reverse direction to that is transported from liver to peripheral tissues through VLDL → LDL cycle.

Process

HDL is synthesized in liver and small intestine. Nascent HDL contain phospholipids and unesterified cholesterol and Apo-A, C, E. This nascent HDL is secreted into circulation where it acquires additional unesterified cholesterol from peripheral tissues. Within the HDL particle, the cholesterol is esterified by lecithin – cholesterol acetyltransferase (LCAT) to form cholesteryl ester and additional lipid are transported to HDL from VLDL and chylomicrons. Apo-A1 activates LCAT.

Q. 6

Lipoprotein associated with carrying cholesterol from peripheral tissues to liver is ‑

A

HDL

B

LDL

C

VLDL

D

IDL

Q. 6

Lipoprotein associated with carrying cholesterol from peripheral tissues to liver is ‑

A

HDL

B

LDL

C

VLDL

D

IDL

Ans.

A

Explanation:

HDL particles transport cholesterol from extrahepatic tissues to liver (i.e. reverse cholesterol transport) which is then excreted through bile.